Modulation of Human Neutrophil Adherence by Periodontopathic Bacteria: Reversal by Specific Monoclonal Antibodies

Seow, W.K.; Bird, P. S.; Seymour, G. J.; Thong, Y.H.

doi:10.1159/000234995

Cited by 14 publications

(6 citation statements)

References 13 publications

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“…Some periodontal bacteria such as P. gingivalis, Actinobacillus actinomycetemcomitans and Fusobacterium nucleatum are capable of evading neutrophils using a number of mechanisms. These organisms have been shown to inhibit some of the protective functions of neutrophils such as phagocytosis, chemotaxis, production of superoxide dismu- tase, adherence and direct leukocytotoxicity (1,31,36). Reife et al (29) have shown recently that P. gingivalis could not induce an immediate inflammatory response in a mouse model, thus evading the innate host defense mechanisms and in the present study, neutrophil maximal infiltration did not occur for several days in control mice, suggesting neutrophil evasion by P. gingivalis.…”

Section: Discussionmentioning

confidence: 99%

Immunohistological study of lesions induced by Porphyromonas gingivalis in a murine model

Gemmell

Bird

Bowman

et al. 1997

Oral Microbiology and Immunology

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A previous study used a mouse model to demonstrate protection after challenge with Porphyromonas gingivalis ATCC 33277. In the present study, this same model was used to determine the phenotype of cells recruited into the lesions during the course of the protective immune response after immunization with this periodontal pathogen. BALB/c mice were immunized with 100 micrograms of P. gingivalis outer membrane antigens per mouse weekly for 3 weeks followed by challenge with live organisms 3 weeks after the final immunization. Hematoxylin and eosin-stained sections showed inflammatory infiltrates in all lesions from control (immunized with adjuvant only) and immunized mice. The lesions developed central necrotic cores surrounded by neutrophils, phagocytic macrophages and lymphocytes. Neutrophils were the predominant cells in the lesions 1 day after challenge with significantly more in immunized than control mice. Acid phosphatase and nonspecific esterase-positive macrophages were detected at day 4 and became the predominant cells in the healing lesions. CD4- and CD8-positive T-cells were present from day 1, and while numbers increased over time, there were no significant differences in control or immunized mice. When mice were depleted of CD4 or CD8 cells prior to immunization with P. gingivalis, fewer neutrophils were found in the lesions 1 day after challenge compared with undepleted immunized mice. Acid phosphatase and nonspecific esterase-positive macrophages were not affected by T-cell depletion. The results suggest that the P. gingivalis-induced lesion in immunized BALB/c mice is consistent with a strong innate immune response involving the recruitment of neutrophils in the first instance which may be under the control of T cells. This is followed by the infiltration of phagocytic macrophages which are involved in the healing process and do not appear to be regulated by T cells.

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Section: Discussionmentioning

confidence: 99%

Immunohistological study of lesions induced by Porphyromonas gingivalis in a murine model

Gemmell

Bird

Bowman

et al. 1997

Oral Microbiology and Immunology

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“…The presence of increased numbers of P. gingivalis cells in periodontal pockets has been associated with chronic suppurative lesions and progressive periodontal destruction (48). It has been speculated that this destruction is mediated, in part, by alterations that occur in the function of the large numbers of PMN that are found in and around periodontal pockets (45,58). The PMN migrate through the mucosal lining of the pocket and are essential for the defense of periodontal tissues against the mixed microflora that constitutes subgingival plaque (11).…”

mentioning

confidence: 99%

Depolarization of polymorphonuclear leukocytes by Porphyromonas (Bacteroides) gingivalis 381 in the absence of respiratory burst activation

Novak

Cohen

1991

Infect Immun

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Bacteroides spp. may contribute to the chronicity of mixed infections by affecting the normal functions of polymorphonuclear leukocytes (PMN). This study evaluated the physiologic and biochemical responses of human peripheral blood PMN to a variety of strains of the oral periodontal pathogen Porphyromonas (Bacteroides) gingivalis. Strain 381 and ATCC type strain 33277 caused rapid and lasting depolarization of the electrochemical potential that exists across the PMN membrane by a mechanism that was independent of activation of the pertussis toxin-sensitive G protein or protein kinase C. Membrane depolarization did not initiate increases in intracellular calcium or respiratory burst activation, and activity was not inhibited by surface proteolysis or sugars. However, membrane depolarization was associated with inhibition of PMN responses to the chemotactic peptide N-formylmethionyl leucyl phenylalanine. Membrane-depolarizing activity was isolated with the outer membrane of strain 381 by surface extraction of the bacteria by using Zwittergent 3,14, followed by Sephacryl S-200 gel filtration chromatography. The partially purified outer membrane components were heat stable, were not inhibited by tosyl-lysine chloromethyl ketone, and inhibited N-formylmethionyl leucyl phenylalanine-stimulated superoxide production. The results suggest that outer membrane components of P. gingivalis 381 and 33277 have porinlike activity that can depolarize PMN membranes and immobilize PMN responses to chemotactic peptides. This may prove to be an important virulence characteristic of these strains. * Corresponding author. t Present Address: Department of Periodontics, University of Texas Health Sciences Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78284-7894.cidal respiratory burst. The purpose of this study was to characterize the physiological and biochemical responses of human PMN to selected strains of the periodontal pathogen P. gingivalis to gain an insight into how the presence of this microorganism may affect PMN and, subsequently, periodontal disease progression. MATERIALS AND METHODSBacterial strains and growth conditions. P. gingivalis 381, ATCC 33277, W83, and W50 and rifampin-resistant 3079.03-Rl were grown to the late-logarithmic-early-stationary phase in prereduced Schaedler broth (Oxoid, Basingstoke, England) containing hemin at 10 ,ug-ml-'. The purity of cultures was ascertained by phase-contrast microscopy and Gram staining and confirmed by aerobic and anaerobic subculturing on blood agar plates, followed by biochemical analysis using API ZYM chromogenic substrates (Analytab Products, Plainview, N.Y.). Cells were harvested by centrifugation, washed twice in sterile, isotonic saline, lyophilized, and stored at -20°C. Immediately prior to use, bacterial samples were suspended at 1 mg (dry weight) ml-' in Kreb-Ringer phosphate, pH 7.4 (KRP) and dispersed by vortexing and intermittent 30-s bursts of sonication at 50 W at 4°C in a Braun-sonic 1510 homogenizer (B. Braun, AG, Melsungen, Germany) until a sing...

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“…The nature of this ligand is unknown, but the development of specific monoclonal antibod ies which can interfere with ligand-receptor interac tion, as has been done with anaerobic bacteria [21], and the incorporation of the monoclonal antibody into an affinity chromatography procedure, may be a useful experimental approach to take.…”

Section: Discussionmentioning

confidence: 99%

Direct Activation of Human Polymorphonuclear Leukocytes by <i>Pseudomonas aeruginosa</i>

Mai

Seow²,

McCormack³

et al. 1989

Int Arch Allergy Immunol

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Brief exposure of polymorphonuclear leukocytes (PMNs) to unopsonized Pseudomonas aeruginosa resulted in significant enhancement of PMN adherence and ³H-deoxyglucose uptake, two important indicators of PMN activation. Dose-response and time-course experiments show that maximal stimulation of PMNs occurred at a PMN: bacteria ratio of 10:1 and exposure time of 10 min. The PMN-stimulatory capacity of P. aeruginosa was completely or partially abolished by treatment with formalin, heat, ultrasonication and ultraviolet (UV) irradiation, all of which affect the integrity of ligands on the bacteria surface. The putative glycoprotein ligand(s) contains galactose rather than glucose as shown by the ability of galactose in the medium to abrogate PMN-stimulatory activity. This PMN-stimulatory activity was not mediated by soluble factor(s) released from either P. aeruginosa or PMNs as shown by experiments with appropriate supernatants. Finally, PMN-stimulating activity was also observed with P. maltophilia and P. pseudomallei, but not by the other Pseudomonas spp. such as P. cepacia and P.Buorescens. These results suggest that P. aeruginosa and other Pseudomonas spp. may have little capacity to circumvent PMN host defences. This may account in part for their limited pathogenic role as opportunistic micro-organisms, for the severe inflammatory lesions seen in Pseudomonas infections when they do occur, and is consistent with the fact that infection with these organisms is commonly associated with impaired quantity or function of PMNs.

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Modulation of Human Neutrophil Adherence by Periodontopathic Bacteria: Reversal by Specific Monoclonal Antibodies

Cited by 14 publications

References 13 publications

Immunohistological study of lesions induced by Porphyromonas gingivalis in a murine model

Immunohistological study of lesions induced by Porphyromonas gingivalis in a murine model

Depolarization of polymorphonuclear leukocytes by Porphyromonas (Bacteroides) gingivalis 381 in the absence of respiratory burst activation

Direct Activation of Human Polymorphonuclear Leukocytes by <i>Pseudomonas aeruginosa</i>

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